Timothy C. Hain, MD
Return to OtoNeurology Education Index. Please read our disclaimerVitamin B12 deficiency is common in the population over 80 (about 10%). It can be a cause of unsteady gait (ataxia), sometimes accompanied by anemia (macrocytic), and loss of position sense. When associated with spinal cord disease, it is sometimes termed "subacute combined degeneration". The ataxia is called a "sensory ataxia", because it appears to be related to loss of position sensation from the feet. A list of diseases that can present with a similar picture is given below:
The term subacute combined degeneration was coined by Russell, Batten and Collier in 1900 to describe pathological changes in the spinal cord. While changes in the posterior columns are emphasized in clinical accounts, pathologically the lateral and anterior columns are also often affected. The peripheral nerves are generally unaffected.
B12 is available only from animal sources and thus strict vegetarians are at a risk of deficiency. B12 is bound to animal protein and released by gastric acid. Gastric conditions contributing to B12 deficiency include pancreatic deficiency states, ileal disease (e.g. Crohn's disease), and surgery such as gastrectomy. Pernicious anemia accounts for 15-70% of B12 deficiency. In this situation it is an autoimmune disorder where antibodies are made to intrinsic factor. Drugs that reduce stomach acidity and gastritis are other causes. Because B12 is stored in the liver, it takes about 2 years following a sudden cessation of intake for signs of deficiency to arise.
B12 deficiency is usually detected through a B12 level. Typical lower limits of normal are 200 pg/ml. Levels between 150 and 300 should be confirmed with secondary surrogate markers (see following).
Surrogate markers include methylmalonic acid (MMA) and homocysteine. MMA is elevated in 90-98% of patients with B12 deficiency. This test may be overly sensitive as 25-20% of patients over the age of 70 have elevated levels of MMA, but 25-33% of them do not have B12 deficiency. For this reason, MMA is not routinely recommended in the elderly. Homocysteine is also elevated in B12 deficiency.
In the past, the Shilling's test was advocated as a method of determining whether oral or intramuscular B12 supplementation will be required. In the Shillings test it can be determined whether or not oral B12 is absorbable using a radioassay. The Shillings test is, however, somewhat expensive and certainly inconvenient. Some authors advocate simply providing B12 to the patient via an oral or nasal route, and then retesting the patient after a few months as a simpler and more direct method of determining whether shots will be needed.
While B12 deficiency can cause a macrocytic anemia, this is not required for diagnosis, and the absence of anemia should not dissuade the physician from considering B12 deficiency.
There are presently a variety of options. Oral therapy involves giving 250 ug to 1 mg of B12 daily. Monthly injections of B12 are traditional. Nasal B12 is also now available. All modes of treatment should include a method of checking for response. If clinical syndromes do not improve on oral B12 supplementation, asess surrogate markers (MMA, homocysteine), or perform a Shilling test.
A 45 year old man presented with dizziness. The usual tests including audiometry, ENG and an MRI were all normal. In the course of an evaluation for gastritis it was determined that he was infected with H-pylori. B12 levels were checked and found to be low (100). His dizziness eventually resolved with injections of B12.